Genetic evidence that mutants of the methoprene-tolerant gene of Drosophila melanogaster are null mutants.
The Methoprene-tolerant (Met) mutation of Drosophila melanogaster results in resistance to juvenile hormone ( JH) or JH analogs and appears to alter JH reception during late larval development. Several alleles of Met have been recovered from methoprene selection screens after mutagenesis with ethyl methanesulfonate, X-rays, or transposable genetic elements. The phenotype of files carrying any of these alleles is similar-resistance to the toxic and morphogenetic effects of methoprene-but otherwise is essentially wild-type. Understanding the function of the Met gene requires that we know whether these alleles are hypomorphic, producing some functional gene product, or amorphic, producing no functional gene product. This determination was made by comparing the methoprene-resistance phenotype produced by representative Met alleles with that produced by a chromosome carrying a deficiency that deletes the Met gene. The level of resistance to either the toxic or the morphogenetic effect of methoprene was similar among files heterozygous for either the deficiency chromosome or for any of the alleles. The results provide genetic evidence that the Met alleles recovered to date are amorphic and suggest that the Met gene may not be mutable to a more severe Met allele that affects the viability, development, or reproduction of the flies.[1]References
- Genetic evidence that mutants of the methoprene-tolerant gene of Drosophila melanogaster are null mutants. Wilson, T.G. Arch. Insect Biochem. Physiol. (1996) [Pubmed]
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